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Journal of Pharmacology And Experimental Therapeutics, Vol. 147, Issue 2, 186-193, 1965
Copyright © 1965 by American Society for Pharmacology and Experimental Therapeutics


"FALSE NEUROCHEMICAL TRANSMITTERS" AND THE MECHANISM OF SYMPATHETIC BLOCKADE BY MONOAMINE OXIDASE INHIBITORS

I. J. Kopin 1, J. E. Fischer 1, J. M. Musacchio 1, W. D. Horst 1, and Virginia K. Weise 1

1 Laboratory of Clinical Science, National Institute of Mental Health, National Institutes of Health, Department of Health, Education and Welfare, Bethesda, Maryland

Following administration of tyramine-H3 or m-tyramine-H3 the beta-hydroxylated derivatives of these amines, octopamine-H3 and m-octopamine -H3, are rapidly formed in the heart and salivary gland. Formation of the beta - hydroxylated derivatives is enhanced by inhibition of monoamine oxidase, but agr-methyloctopamine-H3 formation from agr-methyltyramine-H3 is uninfluenced. Octopamine-H3 formation and endogenous octopamine accumulation after monoamine oxidase inhibition are largely prevented by chronic sympathetic denervation. Octopamine in tissues is released by sympathetic nerve stimulation, but this amine is relatively inactive. The hypothesis is proposed that the partial sympathetic blockade observed after chronic inhibition of monoamine oxidase or after administration of large doses of tyramine may be the consequence of replacement of norepinephrine by a false, inactive neurochemical transmitter.

Accepted on October 13, 1964




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Copyright © 1965 by the American Society for Pharmacology and Experimental Therapeutics.